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"Thomas, F"
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The Roman Inquisition on the Stage of Italy, c. 1590-1640
From the moment of its founding in 1542, the Roman Inquisition acted as a political machine. Although inquisitors in earlier centuries had operated somewhat independently of papal authority, the gradual bureaucratization of the Roman Inquisition permitted the popes increasing license to establish and exercise direct control over local tribunals, though with varying degrees of success. In particular, Pope Urban VIII's aggressive drive to establish papal control through the agency of the Inquisition played out differently among the Italian states, whose local inquisitions varied in number and secular power. Rome's efforts to bring the Venetians to heel largely failed in spite of the interdict of 1606, and Venice maintained lay control of most religious matters. Although Florence and Naples resisted papal intrusions into their jurisdictions, on the other hand, they were eventually brought to answer directly to Rome-due in no small part to Urban VIII's subversions of the law.
Thomas F. Mayer provides a richly detailed account of the ways the Roman Inquisition operated to serve the papacy's long-standing political aims in Naples, Venice, and Florence. Drawing on the Inquisition's own records, diplomatic correspondence, local documents, newsletters, and other sources, Mayer sheds new light on papal interdicts and high-profile court cases that signaled significant shifts in inquisitorial authority for each Italian state. Alongside his earlier volume,The Roman Inquisition: A Papal Bureaucracy and Its Laws in the Age of Galileo, this masterful study extends and develops our understanding of the Inquisition as a political and legal institution.
eBook
The stronghold : how Republicans captured Congress but surrendered the White House
\"Once the party of presidents, the GOP in recent elections has failed to pull together convincing national majorities. Republicans have lost four of the last six presidential races and lost the popular vote in five of the last six. In their lone victory, the party incumbent won- during wartime- by the slimmest of margins. In this fascinating and important book, Thomas Schaller examines national Republican politics since President Ronald Reagan left office in 1989. From Newt Gingrich's ascent to Speaker of the House through the defeat of Mitt Romney in 2012, Schaller traces the Republican Party's institutional transformation and its broad consequences, not only for Republicans but also for America. Gingrich's \"Contract with America\" set in motion a vicious cycle, Schaller contends: as the GOP became more conservative, it became more Congress-centered, and as its congressional wing grew more powerful, the party grew more conservative. This dangerous loop, unless broken, may signal a future of increasing radicalization, dependency on a shrinking pool of voters, and less viability as a true national party. In a thought-provoking conclusion, the author discusses repercussions of the GOP decline, among them political polarization and the paralysis of the federal government\"-- Provided by publisher.
Book
Impact of oncogenic pathways on evasion of antitumour immune responses
Immunotherapeutic interventions are showing effectiveness across a wide range of cancer types, but only a subset of patients shows clinical response to therapy. Responsiveness to checkpoint blockade immunotherapy is favoured by the presence of a local, CD8+ T cell-based immune response within the tumour microenvironment. As molecular analyses of tumours containing or lacking a productive CD8+ T cell infiltrate are being pursued, increasing evidence is indicating that activation of oncogenic pathways in tumour cells can impair induction or execution of a local antitumour immune response. This Review summarizes our current knowledge of the influence of oncogenic effects on evasion of antitumour immunity.
Journal Article
Melanoma-intrinsic β-catenin signalling prevents anti-tumour immunity
Only a subset of patients with melanoma responds to new immunotherapeutic therapies; here, β-catenin signalling is identified as an important pathway that confers resistance to this type of approach, with implications for future treatment strategies.
WNT/β-catenin target in drug-resistant melanoma
Only a subset of patients with melanoma responds to the new wave of immune-based therapies. Here Stefani Spranger
et al
. identify active WNT/β-catenin signalling as a common feature in melanomas showing resistance to immunotherapies that act via checkpoint blockage by anti-PD-L1 or anti-CTLA-4, a phenomenon associated with the exclusion of T cells from the tumour microenvironment. This work points to β-catenin as an example of specific oncogenic signal that could be targeted as part of an anti-tumour treatment strategy.
Melanoma treatment is being revolutionized by the development of effective immunotherapeutic approaches
1
,
2
. These strategies include blockade of immune-inhibitory receptors on activated T cells; for example, using monoclonal antibodies against CTLA-4, PD-1, and PD-L1 (refs
3
,
4
,
5
). However, only a subset of patients responds to these treatments, and data suggest that therapeutic benefit is preferentially achieved in patients with a pre-existing T-cell response against their tumour, as evidenced by a baseline CD8
+
T-cell infiltration within the tumour microenvironment
6
,
7
. Understanding the molecular mechanisms that underlie the presence or absence of a spontaneous anti-tumour T-cell response in subsets of cases, therefore, should enable the development of therapeutic solutions for patients lacking a T-cell infiltrate. Here we identify a melanoma-cell-intrinsic oncogenic pathway that contributes to a lack of T-cell infiltration in melanoma. Molecular analysis of human metastatic melanoma samples revealed a correlation between activation of the WNT/β-catenin signalling pathway and absence of a T-cell gene expression signature. Using autochthonous mouse melanoma models
8
,
9
we identified the mechanism by which tumour-intrinsic active β-catenin signalling results in T-cell exclusion and resistance to anti-PD-L1/anti-CTLA-4 monoclonal antibody therapy. Specific oncogenic signals, therefore, can mediate cancer immune evasion and resistance to immunotherapies, pointing to new candidate targets for immune potentiation.
Journal Article
Playing to the camera : musicians and musical performance in documentary cinema
Playing to the Camera is the first full-length study devoted to the musical performance documentary. Its scope ranges from rock concert films to experimental video art featuring modernist music. Unlike the \"music under\" produced for films by unseen musicians, on-screen \"live\" performances show us the bodies that produce the sounds we hear. Exploring the link between moving images and musical movement as physical gesture, this volume asks why performance is so often derided as mere skill whereas composition is afforded the status of art, a question that opens onto a broader critique of attitudes regarding mental and physical labor in Western culture.--Publisher's website.
Book
Multidrug-Resistant Candida: Epidemiology, Molecular Mechanisms, and Treatment
Invasive Candida infections remain an important cause of morbidity and mortality, especially in hospitalized and immunocompromised or critically ill patients. A limited number of antifungal agents from only a few drug classes are available to treat patients with these serious infections. Resistance can be either intrinsic or acquired. Resistance mechanisms are not exchanged between Candida; thus, acquired resistance either emerges in response to an antifungal selection pressure in the individual patient or, more rarely, occur due to horizontal transmission of resistant strains between patients. Although multidrug resistance is uncommon, increasing reports of multidrug resistance to the azoles, echinocandins, and polyenes have occurred in several Candida species, most notably Candida glabrata and more recently Candida auris. Drivers are overall antifungal use, subtherapeutic drug levels at sites of infection/colonization, drug sequestration in the biofilm matrix, and, in the setting of outbreaks, suboptimal infection control. Moreover, recent research suggests that DNA mismatch repair gene mutations may facilitate acquisition of resistance mutations in C. glabrata specifically. Diagnosis of antifungal-resistant Candida infections is critical to the successful management of patients with these infections. Reduction of unnecessary use of antifungals via antifungal stewardship is critical to limit multidrug resistance emergence.
Journal Article
The host STING pathway at the interface of cancer and immunity
A major subset of human cancers shows evidence for spontaneous adaptive immunity, which is reflected by the presence of infiltrating CD8+ T cells specific for tumor antigens within the tumor microenvironment. This observation has raised the question of which innate immune sensing pathway might detect the presence of cancer and lead to a natural adaptive antitumor immune response in the absence of exogenous infectious pathogens. Evidence for a critical functional role for type I IFNs led to interrogation of candidate innate immune sensing pathways that might be triggered by tumor presence and induce type I IFN production. Such analyses have revealed a major role for the stimulator of IFN genes pathway (STING pathway), which senses cytosolic tumor-derived DNA within the cytosol of tumor-infiltrating DCs. Activation of this pathway is correlated with IFN-β production and induction of antitumor T cells. Based on the biology of this natural immune response, pharmacologic agonists of the STING pathway are being developed to augment and optimize STING activation as a cancer therapy. Intratumoral administration of STING agonists results in remarkable therapeutic activity in mouse models, and STING agonists are being carried forward into phase I clinical testing.
Journal Article